Background Atrial fibrillation (AF) was used to be considered as nongenetics disorder, but recent studies have revealed that genetics variants conferred susceptibility to AF development, but most with limited evidence. In order to systematically evaluate the overall contributions of gene-disease association studies to current understandings of the genetic susceptibility to atrial fibrillation, we perform a systematic review and meta-analysis based on comprehensive searches. Method All studies on the associations of genetics variants with AF risk were identified by searching the following databases: Medline, Embase, BIOSIS, Global Health, LILACS and CBMDisc. Odds ratios (CI) and 95 % confidence intervals (CI) were calculated under homozygote comparison (HC), dominant model (DM) and recessive model (RM), respectively. Results A total of 41 studies on 32 genes and 72 polymorphisms locations were identified. The summary OR was statistically significant associations in 23 (31.94 %) single nucleotide polymorphisms (SNPs). The genes in renin-angiotensin-aldosterone system (RAAS) and ion channels were the mostly studied. Four SNPs (50.00 %) in RAAS genes were significantly associated with AF susceptibility: ACE I/D (HC: OR = 1.53, 95 % CI: 1.14-2.0 DM: OR = 1.47, 95 % CI: 0.86-1.53; RM: OR = 0.49, 95% CI: 0.41-0.59); AGT A-20C (HC: OR = 1.56, 95 % CI: 1.41-2.12); AGT M235T (HC: OR = 2.37, 95 % CI: 1.21-4.65). Statistically significant associations were also found in the following genes and SNPs: ABCA1 G1051A, BCHE G1615A, CETP A1061G, I405V, TaqIB, CRP C1444T, EDN2 A985G, eNOS T-786C, IL-10 T-819C, A-592C, MinK G38S, KCNH2 rs1805120, Kir 3.4 C171T, G810T, MMP2 C-1306T, Factor Ⅱ G20210A, SCN5A H58R, SLC26A8 I639V, G-protein β-subunit C825T, chromatosome 4q25 rs2200733 and rs10033464. Conclusions Nearly one-third of SNPs were statistically significant associated with AF risk, with variants in RAAS genes most highly significant association. More studies on a wide range of genes are merited. Background Atrial fibrillation (AF) was used to be considered as nongenetics disorder, but recent studies have revealed that genetics variants conferred susceptibility to AF development, but most with limited evidence. In order to systematically evaluate the overall contributions of gene-disease association studies to current understandings of the genetic susceptibility to atrial fibrillation, we perform a systematic review and meta-analysis based on comprehensive searches. Method All studies on the associations of genetics variants with AF risk were identified by searching the following databases: Medline, Embase, BIOSIS, Global Health, LILACS and CBMDisc. Odds ratios (CI) and 95% confidence intervals (CI) were calculated under homozygote comparison (HC), dominant model (DM) and recessive model 32 summary and 72 polymorphisms locations were identified. The summary OR was found significant associations in 23 (31.94%) single n The genes in renin-angiotensin-aldosterone system (RAAS) and ion channels were the most studied. Four SNPs (50.00%) in RAAS genes were significantly associated with AF susceptibility: ACE I / D = 1.53, 95% CI: 1.14-2.0 DM: OR = 1.47, 95% CI: 0.86-1.53; RM: OR = 0.49, 95% CI: 0.41-0.59); AGT A-20C Statistically significant associations were also found in the following genes and SNPs: ABCA1 G1051A, BCHE G1615A, CETP A1061G, I405V (HC: OR = 2.37, 95% CI: 1.21-4.65) , TaqIB, CRP C1444T, EDN2 A985G, eNOS T-786C, IL-10 T-819C, A-592C, MinK G38S, KCNH2 rs1805120, Kir 3.4 C171T, G810T, MMP2 C- 1306T, Factor II G20210A, SCN5A H58R, SLC26A8 I639V, G-protein β-subunit C825T, chromatosome 4q25 rs2200733 and rs10033464. Conclusions Nearly one-third of SNPs were significantly associated with AF risk, with variants in RAAS genes most highly significant association. More studies on a wide range of g enes are merited.